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B cells modulate inflammation in tuberculosis

The contribution of B lymphocytes, which are key players in immunity against infection, is still poorly understood in the context of tuberculosis. Researchers at the Institute of Pharmacology and Structural Biology (IPBS  - CNRS/Université Toulouse III - Paul Sabatier) found that B cells modulate tuberculosis-associated inflammation through the production of type I interferon. This study is published in the American Journal of Respiratory and Critical Care Medicine, on November 21 2017.


In addition to their well-known function as antibody-producing cells, B lymphocytes exhibit antibody-independent innate functions in immunity to various diseases of infectious or non-infectious nature. In tuberculosis, B cells accumulate in lungs, yet their functional contribution to host response to this infection remains poorly understood. With the aim to investigate the contribution of B cells in tuberculosis beyond antibody production, the researchers investigated the global transcriptomic changes in B cells isolated from Mycobacterium tuberculosis-infected mice. The study revealed these B cells displayed a STAT1-centered signature, suggesting a role for interferons in B cell response to infection. It was found that the in vitro production of type I interferon by B cells involved the innate sensor STING, and was antagonized by MyD88 signaling. Importantly, in vivo experiments confirmed that B cells expressed type I interferon in the lungs of M. tuberculosis-infected mice and, more importantly and of clinical relevance, in pleural fluid from patients with tuberculosis. What is the consequence of this type I interferon expression by B cells? The researchers found that it induced an altered polarization of macrophages towards a regulatory/anti-inflammatory profile in vitro. In vivo, an increased provision of type I interferon by B cells in a murine model of B cell-restricted MyD88-deficiency was associated with an enhanced accumulation of anti-inflammatory macrophages during M. tuberculosis infection.

Overall the study identified a novel role for B cells in the immune response to M. tuberculosis, beyond antibody production.


Read the Press release (in French)



Bénard A, Sakwa I, Schierloh P, Colom A, Mercier I, Tailleux L, Jouneau L, Boudinot P, Al-Saati T, Lang R, Rehwinkel J, Loxton AG, Kaufmann SHE, Anton-Leberre V, O’Garra A, Sasiain M, Gicquel B, Fillatreau S*, Neyrolles O* and Hudrisier D*. B cells producing type I interferon modulate macrophage polarization in tuberculosis. Am J Respir Crit Care Med Published ahead of print November 21, 2017 


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This work was performed in collaboration with the group of Dr. Simon Fillatreau (Deutsches Rheuma-Forschungszentrum, Leibniz Institute, Berlin, Germany & Institut Necker-Enfants Malades (INEM), Paris, and other teams in France, Germany, the UK, Argentina and South Africa.




B cells modulate macrophage polarization through the production of type I interferon in tuberculosis. During Mycobacterium tuberculosis infection, stimulated B cells detect mycobacterial products and produce type I interferons, a process that is inhibited by MyD88 signaling. Type I interferons induce an immuno-modulatory program in macrophages, which is characterized by an up-regulation of PD-L1 and the anti-inflammatory cytokine interleukin-10. ©Denis Hudrisier & Françoise Viala